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Effects ofStachybotrys chartarum (atra) conidia and isolated toxin on LungSurfactant production and homeostasis
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1998
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Acute Lung InjuryInflammatory Lung DiseaseImmunotoxicologyLung InflammationPathologyCellular PhysiologyOxidative StressMolecular PharmacologyLungsurfactant ProductionRespiratory ToxicologyPulmonary PharmacologyToxicologyFungal BiologyExperimental ToxicologyPharmacologyIsolated ToxinFungal PathogenLung Lavage FluidSurfactant SubfractionsPhysiologyMicrobiologyMedicineCholine Incorporation
This study evaluated the effects of Stachybotrys chartarum conidia and a trichothecene, isosatratoxin-F, on choline incorporation into DSPC by fetal rabbit alveolar type II cells and on alveolar surfactant subtypes in mice. Exposure of fetal rabbit type II cells to S. chartarum conidia at concentrations of 103 to 106 conidia ml−1 significantly depressed [3H] choline incorporation after 24 h of exposure. Exposure of the rabbit cells to 105 to 106 conidia ml−1 also resulted in significantly depressed [3H] choline uptake after 48 h. Additionally, fetal rabbit alveolar type II cells exposed to isosatratoxin-F in concentrations ranging from 10−9 to 10−4 M showed a significant reduction in [3H] choline incorporation into DSPC. Alveolar surfactant phospholipid concentrations in the different metabolic subfractions of lung lavage fluid of mice intratracheally exposed to either 50 μl of 107 ml−1 S. chartarum conidia or 50 μl 10−7 M isosatratoxin-F showed some significant changes at 12, 24, 48, and 72 h post-exposure, compared to the surfactant subfractions of control mice which were either untreated, exposed to saline or to 50 μl of 10−7 ml−1 Cladosporium cladosporioides conidia. In both the S. chartarum- and the isosatratoxin-F-treated mice, exposure significantly increased P10, P100, and S100 phospholipid concentrations, while the P60 phospholipid concentrations were depressed. In contrast, C. cladosporioides-treated mice showed only one significant change in subfraction phospholipid concentration: P60 was depressed at 48 h post-exposure. These results reveal that alveolar type II cells are sensitive to exposure to S. chartarum conidia and to isosatratoxin F. Sensitivity is manifest by alterations in the normal metabolic processing of alveolar surfactant. In exposed mice, this effect appears to involve a significant increase in newly secreted surfactant and an accumulation of the used surfactant forms. Copyright © 1998 John Wiley & Sons, Ltd.